This emerging paradigm implicates that the current ADT with a single therapeutic approach via targeting androgen/AR in the PCa microenvironment may trigger unwanted pathways that promote macrophage infiltration, reprogram macrophages into TAMs with pro-tumour functions, and enhance EMT, all of which eventually result in increasing PCa cell migration/invasion via induced CCL2. The gene discussed is CCL2; the disease is posterior cortical atrophy.